Light signals from the environment are perceived by specific regulatory photoreceptors in the cytoplasmic compartment and transduced by largely unknown mechanisms to the nuclear compartment to control gene expression and cellular development. The long term goal of this research is to dissect the molecular and cellular basis of how light signals are integrated and relayed into the nucleus to achieve the control of the development mode switch, employing the light-regulated seedling development of Arabidopsis thaliana as an experimental system. Both genetic and molecular evidence have suggested-that COP1 (constitutively photomorphogenic 1) encodes a protein which acts inside the nucleus to suppress the photomorphogenic development in darkness, and that light abrogates this repressive action possibly through a cell-specific regulation of its nucleocytoplasmic partitioning. Thus COP1 not only acts as a molecular switch mediating light control of cellular development, it may also directly participate in light signalling crossing the nuclear envelope. Here I propose to extend our current investigation through a combination of genetic, molecular, cell biological, and biochemical approaches. To investigate the cellular basis of COP1 action and its light regulation, we will confirm the proposed light regulation of COP1 nucleocytoplasmic partitioning based on studies with GUS-COP1 fusion by direct immunological examination of native COP1 in light or dark-grown seedlings, and critical evaluation of its role in light control of cellular development. To reveal the biochemical basis of COP1 action in the nucleus, we will use a combination of in vitro and in vivo assays to examine the capability of COP1 to interact with DNA/RNA and activate or repress promoter activity. To identify other cellular components involved this COP1-mediated light control of development mode switch, we will take complementary genetic and molecular approaches. Genetically, we will identify and characterize Arabidopsis mutations which either mimic the COP1 mutant phenotype or modify the phenotype of a temperature sensitive COP1 mutant allele. Molecularly, we will clone and characterize Arabidopsis genes which encode COP1-interactive proteins. Further, the specific roles of other defined cellular components in the COP1-mediated light control of developmental switch will be examined using similar combinatory approaches. Those studies will provide novel insights into the mechanism of light signaling and its control of cellular development. Since many types of human cancers and diseases are caused by the malfunction of cellular signaling processes, it is hoped that the ability to combat those human health problems will be enhanced through improving our general understanding of cellular signaling mechanisms in a model multicellular organism.